Pre-eclampsia Flashcards

1
Q

What are the renal signs of PET?

A

proteinuria (>0.3g/24hr or ACR >=30mg/mmol (or >=0.3mg/mg)), or random dipstick >=2+, or plasma Cr >=97.2micromol/L, or plasma Cr doubling in absence of other renal disease, or oliguria (<500mL/24hrs)

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2
Q

What are the haematological signs of PET?

A

thrombocytopenia (plt <150 x10^9/L), haemolysis (schistocytes or red cell fragments on blood film, raised bilirubin, raised LDH, decreased haptoglobin), DIC

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3
Q

What are the hepatic signs of PET?

A

new onset raised transaminases (>2x ULN) with or without epigastric or RUQ pain

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4
Q

What are the neurological signs of PET?

A

headache
persistent visual disturbance (scotomata, cortical blindness, photopsia, retinal vasospasm)
convulsions (eclampsia)
stroke
hyperreflexia w sustained clonus

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5
Q

What are the pulmonary, cardiac & utero-placental signs of PET?

A

pulm oedema
generalised oedema (incl facial & airway)

IUGR
suspected foetal compromise
abnormal umbi artery doppler waveform analysis
stillbirth

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6
Q

What is mild-moderate HTN in pregnancy?

And severe?

A

2 bps, measured @ least 4hrs apart, SBP >=140mmHg (but <160mmHg) +/- DBP >=90mmHg (but <110mmHg)

Severe is SBP >=160mmHg +/- DBP >=110mmHg (confirmation within mins= sufficient for Dx of severe)

Any SBP >170mmHg= a medical emergency requiring Rx

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7
Q

What’s gestational HTN?

A

New-onset HTN arising after 20/40 gestation without features of PET, resolves within 3/12 postnatal

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8
Q

What’s chronic HTN in pregnancy?

A

HTN (SBP >=140mmHg OR DBP >=90mmHg) confirmed prior to conception or prior to 20/40, including pts w well-managed HTN entering pregnancy

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9
Q

What’s pre-eclampsia? And what are the signs of “significant end organ dysfunction” they refer to?

A

A multi-system disorder, new-onset HTN (SBP>=140mmHg OR DBP >=90mmHg, on 2 occasions, 4 hrs apart in previously normotensive women- if a SBP is >=160mmHg or DBP >=110mmHg, can confirm within mins) with proteinuria (>=30mg/mmol) OR significant end-organ dysfunction with-or-without proteinuria, after 20/40 gestation, in a previously normotensive woman, resolves within 3/12 postpartum

significant end organ dysfunction=g
proteinuria (>=0.3g/24hrs or ACR >=0.3mg/mg or dipstick >=2+)
plt <100 x 10^9/L
LFTs 2x ULN
Cr >97.2micromol/L or doubling in absence of other renal disease
Pulmonary oedema
New-onset persistent severe headache or visual symptoms

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10
Q

What is the Rx goal with acute antihypertensive management for severe PET?

A

SBP 130-150mmHg/80-90mmHg (avoid maternal hypoT)

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11
Q

What dose of labetalol could be used for acute anti-hypertensive Rx? onset & DOA?

A

20mg slow IV over 2mins, can repeat 40-80mg every 10mins to max 300mg as required
Onset is 5-10mins, DOA 4hrs but Cl is prolonged in hepatic dysfunction

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12
Q

What is labetalol?

A

nonselective B1 & B2 & selective alpha1 blocker (more potent B than alpha, lowers SVR but reflex tachycardia is attenuated by B block, still have pre-syn alpha 2 so -ve feedback catecholamine release can occur)

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13
Q

Risks w labetalol?

A

crosses placenta so ?risk foetal brady, hypoT & hyperglycaemia, also it transfers into breastmilk

can get headache, nausea, scalp tingling, orthostatic hypoT (but B block limits the tachycardia), risks brady.
Contraindicated in asthma, chronic airway limitation (bronchospasm)

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14
Q

What pregnancy category are the antihypertensive drugs used for maternal HTN?

A

all C: drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the foetus or neonate without causing malformations

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15
Q

What are contraindications to hydralazine? Adverse effects? Max dose?

A

Direct-acting smooth muscle relaxant, mainly in resistance arterioles, by inhibiting Ca++ release from SR of arterial smooth muscle cells. The reflex tachycardia from VD will incr HR & contractility so avoid if HR >125bpm, myocardial insufficiency, RV heart failure, care if CAD, CVD, hepatic or renal impairment. May cause tachy, flushing, headache, palpitations & with long-term use, oedema & SLE. Max dose 30mg over 24hrs.

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16
Q

Doses of hydralazine?

A

5-10mg over 3-10mins (lower end dose range if foetal compromise), repeat 5mg IV every 20mins as required, onset 5-20mins, half life 3hrs or 45mins in rapid acetylators. max 30mg/24hrs. Consider infusion (starting at 10mg/hr, titrate) if use 20mg, reduce/cease if HR 125bpm.

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17
Q

What’s an oral option for acute management severe HTN in pregnancy? Adverse effects?

A

Nifedipine- 10-20mg IR tablet, onset is 30-45mins, repeat after 45 mins to a max 80mg/day. Also causes myometrial relaxation (DHP CCB). May cause VD, flushing, headaches, hypoT, reflex tachycardia, AV block or other conduction defects

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18
Q

What are the rules of thumb with fluids in PET?

A

large vols (b4 or after birth) risk pulm oedema & worsening peripheral oedema so only consider prior to regional (nil for epidural, <500mL for spinal) or hydralazine or immediate delivery or if oliguric & we suspect volume deficit (postpartum, <80mL UO/4hrs is physiological so don’t require IVT unless serum plasma Cr is rising).
For severe PET:
-in labour: restrict fluid intake to 60-80mL/hr & monitor hourly FBC (*including Mg++ & oxytocin infusions!)
-post-birth: restrict IV crystalloid to 1.5L in the first 24hrs if no other complications, strict FBC

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19
Q

What other obstetric emergency are PET, eclampsia & HELLP a risk for?

A

Primary PPH- consider carbetocin for these pts

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20
Q

What proportion of PET occurs postpartum?

A

40%, de novo postpartum PET most common days 3-6 & in PET, peak postpartum BP is often on days 3-6 (also lever enzymes & thrombocytopenia will often worsen in the first few days after birth before they improve)

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21
Q

In which group of patients with PET are NSAIDs not recommended?

A

Those with severe PET &/or renal impairment (esp if volume depleted)

Should also avoid NSAIDs if significant blood loss, thrombocytopenia or additional risk factors for bleeding

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22
Q

What is HELLP?

A

Indicates severe disease in pre-eclampsia.
-Haemolysis (rare)- microangiopathic haemolytic anaemia with schistocytes/rbc fragments on blood film, other signs haemolytic (elevated LDH, indirect bilirubin, haptoglobin)
-Elevated liver enzymes- transaminases >2x ULN, may have profound clotting defect (check INR)
-Low platelets- <=100 x 10^9/L (common)- consider platelet transfusion if low platelets considered a hazard to operative birth or if significant PN bleeding is attributed to pre-eclamptic thrombocytopenia. Platelet nadir 24-48hrs after delivery.

May be sudden onset, first sign may be seizure, be wary of RUQ pain in pregnant women
85% of women with HELLP have diagnostic criteria for preeclampsia (ie. in 15% there’s no HTN or proteinuria)- thought same pathophysiology as PET (systemic endothelial dysfunction, inadequate placentation)

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23
Q

What are the indications for birth in PET?

A

-Non-reassuring foetal status
-severe IUGR
-HELLP (expectant management is harmful- 6.3% incidence maternal death & increased risk placental abruption. Plan birth as soon as feasible if >34/40 &/or condition deteriorating, in consultation w Obs, physician, anaesthetist +/- haematologist, consider AN CS but this shouldn’t delay delivery)
-Eclampsia
-uncontrollable HTN despite adequate therapy or uncontrollable systemic signs of (eg. deteriorating plt, LFT +/- renal function or persistent neurological symptoms, persistent epigastric pain/N&V w abn LFTs)
-GA >=37/40
-placental abruption
-APO

Ideally stabilise before delivery (eg. eclampsia prophylaxis, control of HTN) & plan vaginal birth unless need CS for obstetric indications (epidural preferred during VD for HTN control, spinal preferred for CS as rapid onset & avoids hypertensive response to intubation)

24
Q

What proportion of births in Oz are impacted by eclampsia?

A

<0.1% (2.6% of women with PET)

25
Q

What are the indications for Magnesium Sulfate in PET?

A

-Eclampsia (to terminate a seizure)

-Seizure prophylaxis (where it may reduce progression to eclampsia by 58%) in severe PET (defined by MAGPIE trial as: SBP >=170mmHg or DBP >=110mmHg) & at least 3+ proteinuria, OR SBP >=150mmHg or DBP >=100mmHg on 2 occasions & at least 2+ proteinuria & at least 2 s&s of “imminent eclampsia”)

-PET with at least 1 sign of CNS irritability

-if pt requires transfer to a higher service for PET management

26
Q

For how long should MgSO4 be used & what’s the dose?

A

Once indicated, antepartum, intrapartum & for 24hrs postpartum.

Loading dose 4g MgSO4 IV over 20mins, then 1g/hr infusion (reduce dose to 0.5g/hr if renal impairment)

27
Q

What is therapeutic & toxic serum Mg++ levels & what are the monitoring requirements with MgSO4?

A

normal Mg++ is 0.7-1.1mmol/L

therapeutic level: 1.7-3.5mmol/L, toxic level >4mmol/L

Monitor for signs of Mg++ toxicity:
-muscle weakness
-serum [] 2-3mmol/L: nausea/vomiting, flushing, headache, lethargy, drowsiness, depressed deep tendon reflexes
-3-5mmol/L: somnolence, hypoCa++, absent DTR, hypotension, brady, ecg changes (eg. flat P, prol PR & QTc & QRS, peaked T, brady)
-if serum level above 5mmol/L: muscle paralysis (flaccid quadriplegia), apnoea & resp failure, complete heart block, cardiac arrest.
Other symptoms= coma, hypoventilation, m weakness

Monitor BP & pulse every 5 mins until stable then 30-minutely, RR & patellar reflexes hourly, temp 2-hourly, continuous CTG & hourly urine output (w strict FBC)

If RR<12, UO <80mL/4hrs or deep tendon reflexes absent, escalate

28
Q

What other electrolyte derangements is hypermagnesemia associated with & what’s the antidote for hypermagnesemia?

A

hypoCa++, hyperK++
Stop infusion, 10% calcium gluconate, 10mL IV over 5 mins

29
Q

While preparing MgSO4, what’s given to control seizures?

A

midaz 5-10mg IV over 2-5mins OR clonazepam 1-2mg IV over 2-5mins OR Diaz 5-10mg IV at 2-5mg/min (max dose 10mg)

30
Q

What do we do if seizure recurs while giving MgSO4?

A

Further 2g IV over 5 mins, can repeat after 2 mins AND either midaz, clonaz or Diaz

31
Q

What are the 4 main priorities in management of eclampsia & how achieve?

A
  1. Prevent maternal & foetal hypoxia & trauma
    -L) lat position, padded bedrails, 100% O2 10L/min via NRB + support airway, plan for delivery when stabilised
  2. Terminate seizure: Mg loading + infusion with midaz/clonaz or Diaz while preparing MgSO4
  3. prevent seizure recurrence: MgSO4 infusion
  4. Control HTN aim 130-150/80-90 (avoid maternal hypotension)
  5. If localising signs or no improvement after control of HTN & seizure, consider neurologist evaluation for potential stroke
32
Q

What are the signs of “imminent eclampsia”?

A

No reliable predictors & can occur even in absence of HTN & proteinuria, can occur ante/intra/post-partum (usually within 24hrs of birth), but “imminent eclampsia”= @ least 2 of:
1. Ongoing or recurring severe headaches
2. Visual disturbance
3. altered consciousness
4. hyperreflexia or sustained clonus

33
Q

Risk factors for pre-eclampsia? (in order of RR)

A

Previous PET (RR 8)
Adolescent pregnancy (RR 7)
SLE (RR 5.5)
Chronic HTN (RR 5)
Assisted reproductive technology- donor egg (RR 4)
Pre-existing DM (RR 3)
FHx PET (RR 2.9)
Twin pregnancy (RR 2.9)
BMI pre-preg >30 (RR 2.8)
Nullip (RR 2.1)
Assisted reproduction- donor sperm (RR 1.6)
Inter-pregnancy interval >=10yrs, age >=40yo, pre-existing maternal conditions (congenital heart defects, renal disease, autoimmune disease, depression/anxiety), foetal triploidy

34
Q

What’s the pathogenesis of PET?

A

Still debated, thought to be a combo of genetic, immunological and maternal/environmental factors with placenta being central to the pathogenesis.

2 stages:

  1. abnormal shallow placentation early in T1, with inadequate transformation of the maternal spiral arteries whereby they are narrow rather than high capacitance high flow vessels. The narrow spiral arteries are prone to athetosis and compromised placental flow & PET placentas have impaired diastolic flow. Atherosclerotic changes also occur in the decidual vessels (decidual vasculopathy).
  2. a “maternal syndrome” in T2 & T3, characterised by excess anti-angiogenic factors (eg. sFLT1)

Uteroplacental ischemia is thought to lead to release of soluble toxic factors in the maternal circulation causing inflammation & endothelial dysfunction drive the hypertensive, multi-organ failure response in stage 2

35
Q

What proportion of pregnant women are affected by pre-eclampsia?

A

5-7%

36
Q

What is pre-eclampsia with severe features?

A

SBP >=160mmHg OR DBP >=110mmHg on 2 occasions at least 4 hrs apart while the pt is on bedrest (BUT should commence antihypertensive Rx even after one reading)

symptoms of CNS dysfunction:
new-onset visual disturbance
severe or persistent headache despite analgesia, not accounted for by another diagnosis

Serum transaminases >2x ULN or severe persistent RUQ or epigastric pain unresponsive to meds, not accounted for by alternative diagnosis

Thrombocytopenia: plt <100 x 10^9/L

Serum Cr >90micromol/L or doubling of serum Cr in absence of other renal disease

Pulm oedema

37
Q

What are some considerations enroute to theatre for delivery of a pt w severe PET?

A

-control of HTN (SBP 130-150 & DBP 80-90mmHg, avoid maternal HTN)
-eclampsia prophylaxis

-plt must be within 2hrs- ideally spinal (avoid hypertensive response to laryngoscopy)
-requires fresh FBC, G&H (risk primary PPH), coags (CORRECT ANY COAGULOPATHY), electrolytes
-requires 2x large-bore IVC (risk PPH, one for meds & one for IVT)
-requires strict FBC

38
Q

What accounts for 15-20% of deaths in eclampsia?

A

stroke

39
Q

Can GTN or sodium nitroprusside infusions be given in PET?

A

wouldn’t give infusion unless other Rx has failed & birth is imminent

GTN acts mainly on venous capacitance vessels & large coronaries, SNP direct-acting nonselective arterial and venous dilator

could give GTN 1.5microg/kg IV

40
Q

Every decision re: birth involves evaluation of relative maternal & foetal risks but at what gestation should we aim to prolong the pregnancy where possible to improve foetal prognosis & what other considerations are there?

A

<34/40
antenatal corticosteroids for fetal lung maturity
if <30/40, MgSO4 for foetal neuroprotection
pt should be retrieved/transferred to high-level obstetric & neonatal care unit

At 34-36+6/40, planned early delivery ass’d w higher rates RDS & NICU- consider expectant monitoring unless clinical deterioration

41
Q

are pts with PET @ higher risk of VTE?

A

yes

42
Q

Contraindications & precautions for magnesium?

A

hypermagnesemia & maternal cardiac conduction defects. precautions= myaesthenia gravis, reduced real function (monitor UO & plasma Mg++)

43
Q

Why may the airway in PET be more difficult?

A

oedema, more prone to bleeding

44
Q

In what situations should neuraxial definitely be avoided?

A

Considering risk spinal epidural haematoma, plt count <50 x 10^9/L, if there are signs of coagulopathy (eg. bleeding from IV sites) or other abnormal coagulation tests (eg. profound LFT derangement, high INR), if the pt has severe PET & no plt count within 2 hrs (both the absolute plt count & TREND in plt count are important considerations), in the etiology of thrombocytopenia is unknown & plt count is 50-70x10^9/L

45
Q

Does CVP correlate well w PCWP in PET?

A

No, so PAC should be placed if measurement of preload is the main objective

46
Q

What’s the etiology of pulmonary oedema in PET?

A

increased pulm vascular hydrostatic pressure, decreased plasma oncotic pressure, LVF, acute severe HTN, iatrogenic volume overload

47
Q

What are some advantages of epidural analgesia in labour with PET?

A

-Superior pain relief cf systemic analgesics
-Attenuation of hypertensive response to labour pain
-reduction in circulating catecholamines
-possible improvement in uteroplacental flow
-provision of means of rapid conversion to surgical neuraxial anaesthesia, avoiding GA, particularly beneficial if predicted difficult airway
-early placement especially important if declining platelet count

48
Q

What are some considerations for epidural catheter removal in PET?

A

check plt count & coag studies- not to remove catheter unless pt in a clinical state that’d allow insertion

49
Q

How may Mg++ impact on GA?

A

potentiates NMBDs

50
Q

Does the evidence suggest that spinal should be avoided in severe PET due to profound hypotension?

A

No. several trials have refuted this & a case-control study suggests that pts w PET are @ lower risk spinal-induced hypoT & have lower ephedrine requirement than non-pre-eclamptic pts

51
Q

What are some considerations with undertaking spinal in PET?

A

Need to know plt count & trend
Lower than usual doses of vasopressors, carefully titrated (choice of vasopressor doesn’t affect maternal or foetal outcomes in PET)
Care w fluid co-loading- minimise (<500mL) for neuraxial & use conservative intra-op fluid (<80mL/hr unless PPH or other complication)

52
Q

What are indications & some specific considerations for GA in PET?

A

-Indicated if plts or coagulopathy prohibit neuraxial, or if other obstetric indication (eg. placental abruption)
-Anticipate difficult airway (airway oedema, higher bleeding risk)- meticulous positioning for pre-oxygenation, have difficult airway equipment & skilled assistant on hand
-If time & severe PET, consider placing art line pre-induction (target SBP <160mmHg & DBP <110mmHg throughout)
-Control BP prior to induction (labetalol 10mg boluses) & then attenuate the hypertensive response to RSI/intubation/emergence (to limit the risk of ICH & APO) with alfentanil 20microg/kg, lignocaine 1mg/kg, propofol 2mg/kg, sux 1mg/kg

-Let paeds know all induction drugs, esp opioids, given

-Mg++ prolongs duration NDNMBDs & causes muscle relaxation, so if giving NDNMBs, must monitor TOFR & give lower dose (eg. 10mg after the sux)

53
Q

What’s a reasonable regimen for induction in PET, BP target & alternative agents to blunt hypertensive response?

A

Art line pre-induction if time, BP target <160mmHg SBP & <110mmHg DBP
labetalol 10mg boluses to get BP to target
alfentanil 20microg/kg
lignocaine 1mg/kg
propofol 2mg/kg
sux 1mg/kg

Other adjuncts:
lignocaine 1-1.5mg/kg
labetalol titrated in 10mg boluses up to 1mg/kg
esmolol 2mg/kg during induction or 1mg/kg with lignocaine
GTN 1.5-2.5mg/kg IV

54
Q

What are “severe features” in preeclampsia? what other condition is pre-eclampsia with severe features ass’d with?

A

SBP >=160mmHg or DBP>=110mmHg

-new-onset CNS dysfunction: cerebral or visual disturbance (incapacitating headache or one that persists or progresses despite analgesic therapy & no alternative Dx, photopsia/scotomata/cortical blindness/retinal vasospasm)
-impaired liver function not accounted for by another Dx, transaminases >2x ULN or severe persistent R) UQ or epigastric pain unresponsive to medication
-thrombocytopenia, alt <100 x 10^9/L
-Cr >=97.2micromol/L or doubling in absence of other renal disease

-ass’d w microangiopathic haemolytic anaemia (schistocytes, incr LDH, incr bilirubin, decr haptoglobin), features also occurring in thrombotic microangiopathy syndromes eg. TTP

55
Q

first and 2nd line antihypertensives for OPD?

A

methyldopa, labetalol
nifedipine, prazosin, hydralazine